14 Nursing Times 05.03.14 / Vol 110 No 10 / www.nursingtimes.
net Nursing Practice Review Diabetes Keywords: Diabetes/Ketoacidosis/ Diabetic complications
This article has been double-blind
peer reviewed Signs of dehydration, including decreased skin turgor, are often seen in DKA A l a m y Authors Georgia Noble-Bell and Alison Cox are diabetes specialist nurses at Kings College Hospital, London. Abstract Noble-Bell G, Cox A (2014) Management of diabetic ketoacidosis in adults. Nursing Times; 110: 10, 14-17. Ketoacidosis is a serious complication of diabetes. It is commonly precipitated by poor adherence to medication, stress and concurrent illness; it can be life threatening if it is not addressed quickly and efectively. This article discusses the pathophysiology, diagnosis and management of the condition, and highlights the nurses role in this.
D iabetic ketoacidosis (DKA) is a serious and potentially life- threatening complication of diabetes (Joint British Diabetes Societies, 2013). It is a complex disordered metabolic state characterised by hypergly- caemia (elevated blood glucose), acidosis (pH imbalance) and ketonaemia (excess ketones in the blood). Although the majority of patients pre- senting with DKA have type 1 diabetes, those with type 2 diabetes can also develop the condition, especially during acute ill- ness (Umpierrez et al, 2002). People from non-Caucasian ethnic groups are more likely to develop DKA in the presence of type 2 diabetes (Yehia et al, 2008). While the incidence of DKA is difcult to establish, population-based studies suggest an annual incidence of 4.6-8.0 epi- sodes per 1,000 patients with diabetes (Faich et al, 1983); the worldwide mortality rate is 2-10% (Yehia et al, 2008). Over the past 20 years, mortality rates in developed countries have fallen from 7.96% to 0.67% (Lin, 2005) due to a better understanding 5 key points 1 The majority of patients presenting with diabetic ketoacidosis have type 1 diabetes 2 Patients with type 2 diabetes can develop DKA, especially during acute illness 3 Infection is the most common precipitating factor for DKA 4 Clinical signs of DKA include polyuria, polydipsia, weakness, fatigue, weight loss, vomiting and abdominal pain 5 DKA is a medical emergency of the pathophysiology of DKA and advances in the clinical management. Many cases could be prevented by better access to medical care, education and effective communication between patients and health professionals during concur- rent illness (Kitabchi et al, 2004). Pathophysiology DKA results from a dysregulation of carbo- hydrates, protein and lipid metabolism (Yehia et al, 2008) and usually occurs as a consequence of absolute or relative insulin deciency accompanied by an increase in counter-regulatory hormones (glucagon, catecholamine, cortisol, growth hormones and epinephrine), which contribute to increased blood glucose levels and insulin resistance. The combination of insulin deciency and increased counter-regulatory hor- mones leads to alteration in glucose pro- duction and use, increased lipolysis (breakdown of fatty acids to form alternate source of energy) and production of ketone bodies (Umpierrez et al, 2002). An increase in hepatic gluconeogenesis (production of glucose from non-carbohydrate sources) and glycogenolysis (breakdown of glycogen to glucose), renal glucose pro- duction and impaired glucose use in peripheral tissues leads to severe hypergly- caemia (JBDS, 2010). An increase in free fatty acids in circulation as a result of lipolysis enhances hepatic production of ketone bodies, which result in keto- naemia and metabolic acidosis (Kitabachi et al, 2004). Dehydration and electrolyte imbal- ances occur in DKA as a result of several mechanisms. Hyperglycaemia causes uid and electrolytes to shift from the In this article... Epidemiology and pathophysiology of diabetic ketoacidosis Guidance on diagnosis, management and complications The nurses role in caring for patients with DKA Diabetic ketoacidosis is a potentially life-threatening complication of diabetes, making it a medical emergency. Nurses need to know how to identify and manage it Management of diabetic ketoacidosis in adults www.nursingtimes.net / Vol 110 No 10 / Nursing Times 05.03.14 15 intracellular to the extracellular space, leading to cellular dehydration and elec- trolyte imbalance. Both hyperglycaemia and high ketone levels also cause osmotic diuresis, resulting in further dehydration; vomiting is commonly associated with DKA and contributes to uid depletion and electrolyte imbalances (JBDS, 2013).
Precipitating factors About one in ve adults with type 1 dia- betes initially present with DKA (Ump- ierrez et al, 2002). Common precipitating factors for DKA in those with established diabetes are infection, poor adherence to medication, psychological stress and con- current illnesses (Umpierrez et al, 2002; Delaney et al, 2000). Infection is the most common precipi- tating factor for DKA and occurs in about 30-50% of adult cases; other acute condi- tions that may precipitate DKA include cerebral vascular accident, alcohol/drug misuse, pancreatitis, myocardial infarc- tion and trauma (Umpierrez et al, 2002). Recent studies have identied the sig- nicance of medication non-adherence and psychological factors in DKA (Ump- ierrez et al, 2002). High incidences of DKA related to medication non-adherence have been identied in subgroups with type 1 diabetes, including young women with psychological problems such as eating dis- orders (Umpierrez et al, 2002). Other risk factors include poor gly- caemic control, clinic non-attendance and lower socioeconomic status (Wright et al, 2009). The JBDS (2010) has also highlighted a lack of self-management skills as another risk factor associated with recurrent DKA. Clinical presentation and diagnosis The metabolic abnormalities associated with DKA develop rapidly (usually within 24 hours), but the signs and symptoms of poor glycaemic control may be evident for several days before this (Kitabchi et al, 2006). These include polyuria, polydipsia, weakness, fatigue and weight loss. Vom- iting and abdominal pain are frequently the presenting symptoms in DKA (Kearney and Dang, 2007). On physical examination, signs of dehydration are often present, including dry mucus membranes, decreased skin turgor, tachycardia and hypotension. In addition the smell of acetone on the breath and deep and laboured breathing (Kuss- maul breathing) may be observed, particu- larly in patients with severe acidosis. This change in breathing is an attempt by the body to correct the metabolic acidosis and compensatory respiratory alkalosis (Yehia et al, 2008; Umpierrez et al, 2002). Mental state can vary from full alertness to pro- found lethargy (Umpierrez et al, 2002). Laboratory investigations Although DKA can be suspected on clin- ical observations, conrmation of the diagnosis is based on laboratory ndings. The syndrome of DKA consists of the biomedical triad of hyperglycaemia, keto- naemia and metabolic acidosis (JBDS, 2013; Umpierrez et al, 2002). The laboratory investigation in DKA includes measure- ment of: Venous blood glucose; Electrolytes, urea, creatinine, osmo- larity and ketones; Urinalysis for ketones; Blood tests for infection markers; Venous blood gas values. Further investigations may be carried out to identify potential infection or myo- cardial infarction as precipitating factors for DKA; these tests may include complete blood count, blood cultures, cardiac enzymes and ECG (Kitabchi et al, 2004). Clinical presentation and laboratory investigations usually provide the infor- mation needed to diagnose DKA. It is important to remember that not all patients who present with ketoacidosis have DKA (Umpierrez et al, 2002) so when diagnosing DKA, other causes of ketosis should be considered, including starva- tion ketosis and alcohol ketoacidosis (Yehia et al, 2008; Umpierrez et al, 2002). Other differential diagnoses include lactic acidosis, renal failure and drug intoxica- tion (Yehia et al, 2008). Box 1 outlines the JBDS (2013) criteria for diagnosing DKA. DKA is a medical emergency and should be managed promptly (JBDS, 2013). It is important to assess for severity to deter- mine the clinical setting in which the patient is to be managed; criteria are out- lined in Box 2. Management The management of patients presenting with DKA includes a full clinical assess- ment, while regular monitoring of vital signs and consciousness levels using the Glasgow Coma Scale is essential (JBDS, 2013). Key areas in the management of DKA include: Restoring circulatory volume; Insulin therapy (xed-rate intravenous insulin infusion); Correcting metabolic acidosis and electrolyte imbalances; Identifying and treating precipitating factors; Early involvement of the diabetes specialist team (JBDS, 2013). Patients exhibiting one or more of these signs should be assessed by a consultant physician and considered for referral to a high dependency unit: Blood ketones >6mmol/L Bicarbonate level <5mmol/L Venous/arterial blood gas <7.0 Hypokalaemia (low potassium) on admission (3.5mmol/L) Glasgow Coma Scale <12 or abnormal AVPU assessment scale Oxygen saturation <92% on air (assuming normal baseline respiratory function) Systolic BP <90mmHg Pulse rate >100 or <60bpm Source: JBDS (2013) Fluid resuscitation with 0.9% sodium chloride Insulin infusion (xed-rate intravenous insulin infusion) at 0.1 unit/kg/hr Close monitoring of vital signs, blood glucose, ketones, electrolytes and blood gases Continue FRIII until DKA has resolved before converting to subcutaneous insulin Give background insulin alongside IV to prevent rebound hyperglycaemia Involve the diabetes specialist team as soon as possible Ketonaemia 3mmol/L (normal values: <0.6) or signicant ketonuria (>2+ on standard urine dipstick) Blood glucose >11mmol/L (normal values: 3.5-7.8mmol/L) or known diabetes Bicarbonate blood levels (HCO 3 ) <15 mmol/L (normal values: 22-26mmol/L) and/or venous pH <7.3 (normal values: 7.35-7.45) Source: JBDS (2013) BOX 2. CRITERIA FOR HIGH DEPENDENCY CARE BOX 3. KEY MANAGEMENT POINTS BOX 1. CRITERIA FOR DIAGNOSING DKA People write thank-you letters for the care received, not for meeting targets Richard Knowles p26 16 Nursing Times 05.03.14 / Vol 110 No 10 / www.nursingtimes.net Key management points are summa- rised in Box 3.
Restoring circulatory volume Fluid replacement is one of the most important initial therapeutic interven- tions in the management of DKA. Patients are usually dehydrated and correcting this decit will result in signicant metabolic improvement (Kitabchi et al, 2004). The aims of uid resuscitation are to: Restore circulatory volume; Clear ketones; Correct electrolyte imbalance (JBDS, 2010). Pulse and blood pressure should be used to assess the severity of dehydration, as hypotension (systolic BP<90mmHg) is likely to be due to low circulatory volume. Other causes such as heart failure, sepsis and factors such as age, sex and medica- tion history should also be taken into con- sideration (JBDS, 2013). Normal saline (0.9% sodium chloride) is recommended for uid resuscitation (JBDS, 2013). Rapid uid replacement is usually required in the rst few hours of treatment; most patients require between 500ml and 1L to be given rapidly (JBDS, 2013). However, the rate of uid replace- ment must be tailored to patients clinical situation. Special attention must be paid to uid balance in patients at high risk of complications these include older people, pregnant women, children and young people (18-25 years), and those with heart and kidney failure (JBDS, 2010). Insulin therapy The aim of insulin therapy in DKA man- agement is to suppress ketogenesis, reduce blood glucose and correct electro- lyte imbalance. Insulin therapy increases peripheral glucose use and decreases hepatic glucose production, thereby low- ering blood glucose concentration. It inhibits the release of free fatty acids from adipose tissues and decreases ketogenesis (Umpierrez et al, 2002). A continuous xed-rate intravenous insulin infusion (FRIII) of 0.1 units/kg/hr is recommended (JBDS, 2013). The recom- mendation for preparation of insulin infu- sion is 50 units of human soluble insulin made up with 50ml normal saline (0.9% sodium chloride) (JBDS, 2013). FRIII should continue until DKA is resolved. When the blood ketones are <0.6mmol/L, pH >7.3 and the patient is able to eat and drink, an appropriate subcutaneous insulin reg- imen should be recommenced (JBDS, 2013). The JBDS (2013) recommends that background insulin should be continued along with the IV insulin infusion to reduce the risk of rebound hyperglycaemia when the IV insulin infusion is discon- tinued. If background insulin is discon- tinued, a subcutaneous dose must be given before the IV insulin infusion is discon- tinued (JBDS, 2013). The conversion to the subcutaneous insulin regimen should be planned around a mealtime; subcutaneous short-acting insulin should be given at the meal and then IV insulin discontinued one hour later (JBDS, 2013).
Correcting metabolic acidosis and electrolyte imbalance The JBDS (2010) recommends the fol- lowing metabolic treatment targets for DKA: Reduction in blood ketones of at least 0.5mmol/L/hr; Increase in venous bicarbonate by 3mmol/L/hr; Reduction in capillary blood glucose by 3mmol/L/hr; Maintenance of serum potassium at 4-5.5 mmol/L. Blood glucose, ketones, electrolytes, including bicarbonate, and venous pH, should be monitored closely at or near the bedside. If the above targets for blood ketones and/or bicarbonate are not reached, the rate of the IV insulin infusion should be increased by 1 unit every hour until met- abolic targets are achieved (JBDS, 2013). Potassium Maintaining normal serum potassium and prevention of hypoglycaemia are impor- tant in the management of DKA as hypoka- laemia (low potassium level) and hyper- kalaemia (high potassium level) are both life-threatening conditions and common complications. Serum potassium is often high on admission but falls rapidly with insulin treatment, so regular monitoring is essen- tial and potassium should be added to IV infusions if serum potassium is <5.5mmol/L (JBDS, 2013). Capillary blood glucose Prevention of hypoglycaemia is vital, so bedside blood glucose monitoring should be performed every 1-2 hours (JBDS, 2010). It is sometimes necessary to give dextrose infusions to stabilise blood glucose levels; this should be given concurrently with the sodium chloride infusions used to correct circulatory volume (JBDS, 2010). To avoid complications related to rapid infusion it is important to monitor uid balance and electrolytes closely. Regular assessment for complications such as cerebral oedema and uid overload is vital (JBDS, 2013).
The diabetes specialist team The JBDS (2010) stipulates that the diabetes specialist team must be involved in the management of every patient admitted with DKA, and referral should be made as soon as possible during the acute phase. The teams involvement is necessary to improve safety and reduce length of stay (Sampson et al, 2006). Team members play an important role in assessing the precipi- tating cause of DKA, acute management, discharge planning, education and follow- up care including psychological support (JBDS, 2010). The best-practice tariffs stipulate that people admitted with DKA must be referred to the diabetes team and be seen by a member of the team within one working day of admission (Price et al, 2013).
The nurses role All health professionals involved in caring for patients with DKA have a responsi- bility to ensure safe delivery of patient care in accordance with local and national clin- ical guidelines. Some of the roles and responsibilities for nurses include: Ongoing clinical assessment of the patient: this involves regular (at least hourly) monitoring of vital signs and level of consciousness during the acute phase (JBDS, 2013).The early warning score system should be used as a guide to determine the patients clinical condition and response to treatment, and escalated to senior or specialist colleagues or medical team as appropriate; Accurate monitoring of uid balance: this includes accurate intake and output charts (JBDS, 2013). Prescribed uids should be administered and patients monitored for signs of complications related to uid overload, dehydration and electrolyte imbalance; Insulin therapy: this should be administered as prescribed; Regular monitoring of capillary blood glucose and ketones: this is required at least hourly (JBDS, 2013) during the acute phase. Nurses should liaise with the medical team for appropriate adjustment to insulin doses as required; Monitoring of metabolic acidosis and electrolytes: this involves liaising with the medical team to ensure blood gases and appropriate blood tests are carried out regularly, results interpreted and Nursing Practice Review www.nursingtimes.net / Vol 110 No 10 / Nursing Times 05.03.14 17 action taken, for example potassium being added to IV infusions if required. Support early referral to the diabetes team: this involves liaising with the medical team to ensure the diabetes team is contacted as soon as possible after admission. Provide psychological support for patients: this includes keeping the patient and relatives fully informed about the patients clinical condition and the care given. Diabetes specialist nurse: this nurse has a key role in providing patient educa- tion including sick-day management (see below) and arranging follow-up support for patients after discharge.
Complications There are many potential areas for error in the management of DKA, so standardised protocols and guidelines are important to reduce risk for complications and manage- ment errors (Quevedo et al, 2001). Table 1 highlights common complications.
Patient education Patients should be taught how to manage blood glucose during periods of illness (sick-day management). This should include specic information about fre- quency of blood glucose monitoring, blood glucose targets, checking for ketones, taking extra quick-acting insulin, appropriate adjustment of insulin doses, identifying early signs and symptoms of DKA and knowing when to contact the dia- betes specialist team (Kitabchi et al, 2004). Follow-up diabetes review Patients should always have a follow-up review with the diabetes specialist team after an episode of DKA. This should include assessment of overall diabetes control and assessment of risk for a recur- rence of DKA. Risk reduction measures may include referrals to support services such as psy- chological services or structured educa- tion such as Dose Adjustment for Normal Eating (DAFNE) to increase diabetes knowledge, self-management skills and overall control. Best-practice tariffs for DKA and hypo- glycaemia recommend that all patients admitted to hospital with DKA should have access to structured education within three months of discharge (Price et al, 2013). Conclusion Management of DKA reduces the risk of mortality and improves clinical outcomes; this includes restoring circulatory volume, insulin therapy, correcting metabolic aci- dosis and electrolyte imbalance, identi- fying and treating precipitating factors and the early involvement of the diabetes specialist team. The availability of standardised proto- cols and guidelines in clinical areas are important to reduce the risk of manage- ment errors. Patient education about sick-day man- agement and communication with dia- betes specialist team are necessary to reduce the risk of DKA recurring. NT References Delaney MF et al (2000) Diabetic ketoacidosis and hyperglycemic hyperosmolar nonketotic syndrome. Endocrinology Metabolic Clinics of North America; 29: 683-705. Faich GA et al (1983) The epidemiology of diabetic ketoacidosis: population-based study. American Journal of Epidemiology; 177: 551-558. Joint British Diabetes Societies (2013) The Management of Diabetic Ketoacidosis in Adults. Malmesbury: JBDS. tinyurl.com/JBDS-2013-adults Joint British Diabetes Societies (2010) The Management of Diabetic Ketoacidosis in Adults. Malmesbury: JBDS. tinyurl.com/JBDS-2010-adults Kearney T, Dang C (2007) Diabetic and endocrine emergencies. Postgraduate Medical Journal; 83; 79-86. Kitabchi AE et al (2006) Hyperglycemic crisis in adult patients with diabetes; a consensus statement from the American Diabetes Association. Diabetes Care; 27: 2739-2748. Kitabchi AE et al (2004) American Diabetes Association: position statement: hyperglycemic crisis in diabetes. Diabetes Care; 27: S94- S102. Lin SF et al (2005) Diabetic ketoacidosis: Comparison of patient characteristics, clinical presentations and outcomes today and 20 years ago. Chang Gung Medical Journal; 28; 24-30. Price H et al (2013) Developing best practice tarifs for diabetic ketoacidosis and hypoglycemia. Practical Diabetes; 30: 1, 6-8. Quevedo SF et al (2001) Improving diabetes care in the hospital using guideline-directed order. Diabetes Spectrum; 14: 226-233. Sampson MJ et al (2006) Trends in bed occupancy for inpatients with diabetes before and after the introduction of a diabetes inpatient specialist nurse service. Diabetic Medicine; 23: 10081015. Umpierrez GE et al (2002) Diabetic ketoacidosis and hyperglycemic hyperosmolar syndrome. Diabetes Spectrum; 15: 28-36. Wright J et al (2009) Diabetic Ketoacidosis (DKA) in Birmingham, UK, 2000- 2009: an evaluation of risk factors for recurrence and mortality. Journal of Diabetes and Vascular Disease; 9: 278-282. Yehia BR (2008) Diagnosis and management of diabetic ketoacidosis in adults. Hospital Physician; 35: 21-26. TABLE 1 . COMMON COMPLICATIONS IN DKA MANAGEMENT Complications Causes Comments Hypoglycaemia Insulin administration Low-dose insulin infusion Check blood glucose hourly and add 10% dextrose IV when level falls below 14mmol/L Hyperglycaemia Interruption of insulin coverage Continue subcutaneous background insulin with IV insulin infusion and Give pre-meal dose of subcutaneous short-acting insulin at least one hour before discontinuing IV insulin infusion Hypokalaemia Insulin administration Monitor potassium at least two-hourly and if less than 5.5mmol/L add potassium supplement to IV uids Fluid overload Intravenous uid Maintain accurate uid balance chart Cerebral oedema Possible due to rapid correction of hyperosmolarity Check serum sodium and osmolarity at least two-hourly Replace uid gradually Thromboembolism Hypercoagulable state and dehydration Limited evidence to support prophylactic anticoagulation Hypoxia/acute respiratory syndrome Decreased osmotic pressure leads to increase lung water content (pulmonary oedema) Add 10% dextrose when glucose is <14mmol/L Monitoring serum sodium and osmolarity regularly Source: JBDS (2010); Yehia et al (2008) Nursing Times.net For more articles on critical care, go to nursingtimes.net/criticalcare
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